Curriculum Vitae

Nama : Hardiono Dr. dr. SpAn KIC.KAKV

Email : h.hardiono@yahoo.com

Riwayat Pendidikan

1978 Dokter – FK Unair

1983 Dokter Spesialis Anestesiologi FK Unair

1997 Konsultan Anestesiologi dan Terapi Intensif

2000 Konsultan Anestesi Kardiovaskular

2016 Doktor Unair

Riwayat Pekerjaan:

1976 sampai sekarang : dosen di Dept Anestesiologi dan Ranimasi FK Unair

2009 sampai sekarang : Ka Instalasi Rawat Intensive RSUD dr Soetomo

2000 sampai sekarang Konsultan Anestesiologi & Terapi Intensive RS Premier Surabaya

2006 – 2015 : Ketua Komite Keselamatan Pasien RSUD dr Soetomo

2006 – 2015 : Ketua Tim Akreditasi RSUD dr Soetomo

 Life Threatening
Electrolyte Abnormalitiy

Hardiono
Consultant in Anesthesiology & Intensive Care
Dept. of Anesthesiology
Airlangga University – dr. Soetomo Hospital
Surabaya
Introduction
Fluid and Electrolyte abnormality are common in
critically ill patients

Fluid and electrolyte balance electrolyte is important

in maintaining homeostasis in the body

Fluid and electrolyte must also be maintained for the

management of many clinical conditions

No specific signs and symptom in electrolyte

imbalance
 Fluid composition
Total Body Water
60 % body weight

Intracellular
40 % body weight

Extracellular
20 % body weight
Interstitial 15 % body weight
Intravascular 5 % body weight
 Distribution of Electrolyte Imbalance
996 patients in the Emergency Departement
Electrolytes Imbalance Number of patients %
Na+ Hyponatremia 600 60
Hypernatremia 52 5
K+ Hypokalemia 152 15
Hyperkalemia 80 8
Ca++ Hypocalcemia 512 51
Hypercalcemia 38 4
Mg++ Hypomagnesemia 52 5
Hypermagnesemia 10 1

Woerld Journal Emergency Medicine 2013, 4(2): 113-116

 SODIUM HOMEOSTASIS
Sodium is the most abundant cation in the body

Work to regulate extracellular and intravascular volume

Sodium determines serum osmolality, which regulates

water flow,

Total amounts of sodium in the body is component of

water balance

Imbalances in sodium : evaluating serum sodium, serum

osmolality and volume status
 Hyponatremia
Sodium concentration < 135 mEq/L
Classification – depend on concentration
Mild hyponatremia : 130 – 134 mEq/L
Moderate hyponatremia : 120 – 129 mEq/L
Severe hyponatremia : < 120 mEq/L

Classification – depend on volume status

Normovolemia
Hypovolemia
Hypervolemia

Duration of Hyponatremia : Acute or Chronic

Causes of Hyponatremia
Diuretics – Thiazide,

Renal Failure

ECF deficit

SIADH

Congestive heart failure

Hypothyroid

Adrenal Insufficiency
Signs and Symptom of Hyponatremia

Severe : seizures, coma, respiratory arrest, obtundation

Mild to moderate : headache, fatigue, nausea, vomiting,

dizziness, confusion, muscle cramps

Need for hospitalization

Acute hyponatremia
Severe Hyponatremia
Symptomatic hyponatremia
Management of Hyponatremia
Goals of Therapy :
Prevent further decline
Decrease ICP
Relieve symptoms
Avoid excessive correction

Rate of correction 0,5 mEq/L in 1 hour, 4 – 6 mEq/L

(first 24 hours)

Rapid correction can induce Osmotic Demyelination

Syndrome, if the raise of sodium > 10 – 12 mEq/L in the
first 24 hours
Management of Hyponatremia
Calculation of Sodium Deficit

Deficit Sodium = 0,6 X Body Weight X ( Na target – Na )

Raising serum sodium 4 – 6 mEq/L over period of few hours

generally alleviate symptoms and prevent herniation.

Hypertonic Saline : NaCl 3% ( 1 L contain Sodium 513 mEq )

Initial dose of NaCl 3% : 50 – 100 ml bolus, total dose of 300

ml over the course of 30 menit – for severe symptomatic
hyponatremia

Maintenance to increase 0,5 mEq/L per hour

Management of hyponatremia
Fluid restriction

Oral salts tablet

Loop diuretics

SIADH : Vasopresin receptor antagonist (Tolvaptan,

Conivaptan)
Cause water diuresis
 Hypernatremia
Sodium concentration > 145 mEq/L

Results from water depletion or increase Sodium intake

Hypernatremia will not develop if thirst is intact and

water is available.

Clinical signs :
Lethargy, weakness, nausea, vomiting, confusion,
irritability
Severe : twitching, seizures , coma ( Na > 158 mEq/L)
Management of Hyponatremia
Goals : administration dilute fluids, limit water loss ,
correction water deficit
Na – Na Target
Water deficit = 0,5 X Body Weight X
Na Target
Lower Sodium concentration by < 12 mEq/L for the first
24 hours

Hypernatremia with Hypovolemia, treat first with NaCl

0,45 % or 0,9% , do not give Dextrose 5%.

After hypovolemia was corrected give Dextrose 5% 3 – 6

ml/Kg/hour to correct hypernatremia.
 Potasium Homeostasis
Most abundant cation intracellular, intracellular
concentration 150 mEq/L. Total body Potassium 50
mEq/Kg BW.

Role of electrical activity of cell membrane

Potassium concentration determined by shift between

intra and extra cellular compartment, regulate by Na-K
ATPase pump, enhanced by Insulin, hypothermia,
alkalosis, catecholamine and Beta adrenergic.
Hypokalemia
Potassium concentration < 3,5 mEq/L

The severity of manifestation of hypokalemia

proportionate to the degree and duration of the
reduction of serum potassium

Clinical manifestation : muscle weakness, ileus,

arrhythmia, Respiratory arrest

Concentration < 2,5 mEq/L induce muscle necrosis ,

< 2 mEq/L cause ascending paralysis.

ECG manifestation in
Hypokalemia
U wave

Flat T wave

Ventricular arrhythmia, especially patient on digitalis

Pulseless Electrical Activity, Asystol.

Management of Hypokalemia
General issues : prevent or treat life threatening
complications, replace potassium deficit, diagnose and
correct underlying disease.

Urgency therapy depend on severity , rate of decline,

comorbid conditions.
 Management of Hypokalemia

Potassium Chloride 20 mmol will increase Potassium concentrtion 0,25 mmol/L

 Hyperkalemia
Concentration > 5,5 mEq/L
Impaired urinary potassium excretion – Kidney disease
Hemolisis, rhabdomyolisis
Drugs that inhibit renin-angiotensin-aldosteron axis,
heparin, succinylcholine
Redistribution ,most commonly occurred in uncontroled
hyperglycemia (DKA).
Clinical manifestation: muscle weakness, paralysis,
cardiac conduction abnormality, cardiac arrhythmia
ECG change in Hyperkalemia
 Management of Hyperkalemia
EFFECT AGENT DOSE ONSET DURATION

Membrane Calcium 50 mg/Kg Immediate 30 – 60

Stabilizer Gluconate 10% minute
Calcium Chloride 10 mg/Kg Immediate
10%
Shifters Insulin (short Glucose 0,5 – 1 g/Kg 20 minutes 4-6 hours
acting) BW, Insulin 0,1
unit/Kg BW
Albuterol 10 – 20 mg in 4 ml NS, 30 minute 2 hours
over 10 minutes
Excreters Furosemide 40-80 mg 15 minutes 2 – 3 hours
Sodium BIcarb 1 – 2 mEq/Kg hours Duration of
infusion
Definitives Dialysis Immediate 3 hours
 Calcium Homeostasis
Important role : Cellular signaling, neuromuscular
function, muscle contractility, hemostasis, enzymatic, cell
division, healing wound
Majority is in the bone (98%), 80% of Calcium Extracellular
is bound to albumin, the other is in active form : ionized
calcium
Regulate by parathyroid hormone, Vit. D and Calcitrol
Normal concentration 8 – 10,2 mg/dL ( 2,2 – 2,5 mmol/L
Ionized Calcium 4 – 4,6 mg/dL ( 1.0 – 1.5 mmol/L)
Corrected Total Calcium =
Measured Ca / 0,8 X (4.0 – Albumin)
 Hypocalcemia
Serum Calcium < 8 mg/dL or Ionized Calcium <1 mmol/L

Symptoms : hoarseness, stridos, laryngeal spasm,

tetany, Trousseau’s sign, Chvostek’s sign

Cardiac effect : decreased myocardial contractility,

heart failure, exacerbate digitalis toxicity

Cause by : hypomagnesemia, Kidney disease, sepsis,

after thyroid surgery, drugs ( aminoglycoside, Dilantin,
Heparin, Theophyllin, estrogen), Massive blood
transfusion
Management of Hypocalcemia
Administration of Calcium
Calcium gluconas must be diluted with D5W or water for
injection
Ca Gluconas 10% : 0,5 – 1 mg/Kg
Ca Chloride 10% : 0,1 – 0,2 mg/Kg

Correct abnormalities in Magnesium, Potassium and pH

simultaneously

Calcium therapy can induce arrhythmia ventricular in

patient with digitalis, should be given slowly, with
continuous ECG monitoring
Hypercalcemia
Serum concentration > 10,5 mg/dL or Ionized > 5,5 mg/dL

Caused by Hyperparathyroidism, Malignancy (lung, kidney,

breast, Multiple myeloma), Milk –alkali syndrome,
Thyrotoxicosis, intoxication of Vit. A and D.

Sign and Symptom : nausea, polyuria, polydipsia, abdominal

pain, ileus, pancreatitis, confusion, coma. Myocardial
depression ( Ca level > 15 mg/dL)
Management of Hypercalcemia
Infusion of Sodium Chloride 0,9%

Diureticum

Calcitonin

Hydrocortison

Pamidronate, Mithramycin, Plicamycin

Treatment of underlying disease

Magnesium Homeosatsis
Second most abundant intracellular cation (after
potassium)
Extracellular Mg bound to serum albumin, Mg level do
not reliably reflect total body Mg stores
Play important role in Enzym cofactor, Phosphat
transfer, muscle contractility, neuron transmission
Imbalance of Magnesium usually tied to sodium, Calcium
and potassium balance
Used in Pre-Eclampsia Eclampsia, Status asthmaticus ,
Tetanus.
Hypomagnesemia
Serum concentration < 1,5 mEq/L
Caused by : decreased absorption, increased loss of Mg
from kidney or intestines, alteration thyroid hormon,
alcoholism, diuretics
Severity
Mild : 1,6 – 1,9
Moderate : 0,8 – 1,2 mEq/L
Severe : < 0,8 mEq/L

Clinical manifestation: arrhythmia (Torsade), Chorea,

tremor, Mental disturbances, vertigo, seizures
 Management of Hypomagnesemia

Severity Concentration Therapy

Mild 1,4 – 1,6 mEq/L 1-2 gram of MgSO4, in 1 – 2 hours

Moderate 0,8 – 1,2 mEq/L 2 – 4 gram of MgSO4 in 4 – 12 hours

Severe < 0,8 mEq/L 4 – 8 gram of MgSO4 in 12 – 24 hours

Hypermagnesemia
Serum Magnesium > 2.2 mEq/L

Most common cause : renal failure

Clinical manifestation related to neuromuscular and

cardiovascular disturbances

Muscular weakness, drowsiness, confusion,

vasodilatation, hypotension

High serum magnesium may produce : depressed LOC,

bradycardia, cardiac arrhythmia, hypoventilation,
cardiorespiratory arrest
Severity hypermagnesemia
Management of Hypermagnesemia
Treated with administration of Calcium
Calcium Chloride 10% (5 – 10 cc) : 500 – 1000 mg - IV

Eliminate ongoing Magnesium intake

Dialysis for severe hypermagnesemia

IV Saline – Diuresis if renal function and cardiovascular

function are normal

Diuresis induce hypocalcemia, will make signs and

symptoms of hypermagnesemia worse.
 PHOSPHAT Homeostasis
Most abundant intracellular anion, mostly found in bone
and soft tissue

Phosphate is needed for bone mineralisation and

cellular structural components, for energy storage,
oxygen transport (2,3 DPG) and acid base balance

Regulate by parathyroid hormon and vitamin D

Normal level 2,5 – 4,5 mg/dL ( 0,8 – 1,4 mmol/L)

 Hypophophatemia
Level < 2,7 mg/dL, Severe level < 1,5 mg/dL

Predispose to development hypophosphatemia :

malnutrition, refeeding syndrome, alcoholism, DKA,
gastrointestinal loss, medications ( diuretics, antacids,
sucralfate)

Symptoms : weakness, arrhythmia, cardiomyopathy,

acute respiratory failure, confusion, prolonged bleeding
time, disturbances of thrombocyte adhesion.
Management of Hypophosphatemia
Treat underlying disease

Treatment dependent on the severity and the presence

of symptoms

Oral Phosphate if serum phosphate 1 – 1,9 mg/dL ( milk

or supplement containing phosphate)

IV therapy if level < 1 mg/dL – give Sodium Phosphate or

Potassium phosphate

Symptomatic hypophosphatemia whatever the level

must be treated immediately
 Management hypophosphatemia

Serum phosphorus level (mg/dL) IV Phosphorous Replacement IV

2 – 2,5 0.08 – 0.016 mmol/Kg
1,5 - 2 0.16 – 0.24 mmol/Kg
1 – 1,5 0.24 – 0.32 mmol/Kg
Less than 1 0.32 – 0.64 mmol/Kg

Potassium Phosphate /Sodium Phosphate

Should be infused over several hours to reduce the risk of thrombophlebitis
And Calcium Phosphate precipitation
Maximum rate 7,5 mmol/hour
 Hyperphosphatemia
Concentration > 4.5 mg/dL

The most common cause is renal insufficiency

Other cause : Enteral or parenteral therapies, acidosis,

hemolysis, rhabdomyolysis, hypoparathyroidism

Clinical manifestation are caused by hypocalcemia

The risk of Calcium – Phosphate precipitation increases

when the product of the serum calcium and
phosphorous concentration exceeds 55 mg/dL
Take home Message